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Query: UMLS:C0149871 (deep vein thrombosis)
 12,364 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The mechanisms of action of three most commonly used antiplatelet agents (aspirin, sulfinpyrazone, dipyridamole) are briefly discussed. Aspirin inhibits the prostaglandin synthetase of platelets irreversibly and thereby blocks the production of prostaglandin endoperoxides and thromboxane A2, which stimulate platelet aggregation. A daily aspirin dose of 200--300 mg is sufficient to achieve this effect. Sulfinpyrazone appears to interfere with the adhesion of platelets to subendothelial structures and atherosclerotic plaques. Dipyridamole increases cyclic AMP in platelets and thus reduces platelet response to aggregating agents. A few of the satisfactorily performed studies on the clinical effectiveness of antiplatelet agents are mentioned. Sulfinpyrazone treatment of patients with myocardial infarction (Killip--classification I and II), starting 25--35 days after the acute myocardial infarction, reduces cardiac mortality and incidence of sudden death for a period of two years. The efficacy of aspirin treatment in coronary artery disease is not yet definitely established. In patients with transient ischemic attacks, particularly males with appropriate carotid lesions, aspirin therapy reduces the frequency of transient ischemic attacks and possibly the incidence of stroke and death. Sulfinpyrazone is ineffective in these patients. Sulfinpyrazone and aspirin are of value in the prevention of thrombosis in straight arterio-venous shunts. Aspirin reduces the frequency of deep venous thrombosis after total hip replacement in males but not in females. In patients with recurrent venous thrombosis, sulfinpyrazone treatment is effective in preventing thrombosis.
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PMID:[Action mechanism and clinical indications for thrombocyte aggregation inhibitors]. 42 7

Small doses of subcutaneous heparin and infusions of dextran both reduce the incidence of fatal pulmonary embolism after elective general surgery. But both methods have disadvantages. Therefore, the protection against deep vein thrombosis afforded by sulfinpyrazone, a drug which can be taken by mouth as well as by injection, was assessed in a prospective study of 119 patients undergoing elective general or urological surgery. The prophylactic administration of sulfinpyrazone was compared with the effects of small doses of sodium heparin and infusions of dextran-70. The 125I-fibrinogen test was carried out in all patients during their hospitalization. Deep vein thrombosis was diagnosed in 13 of 30 patients (43%) who received sulfinpyrazone, in 9 of 29 (31%) receiving dextran-70 and in 2 of 22 (9%) having subcutaneous heparin. The difference between the sulfinpyrazone and heparin groups was statistically significant (p less than 0.01). Sulfinpyrazone in the dose used in this trial was not effective in reducing the incidence of deep vein thrombosis during elective general surgery.
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PMID:Sulfinpyrazone and postoperative deep vein thrombosis. 92 99

The role of platelets in the initation of arterial thrombosis is clear. In venous thrombosis as well, platelets may in some circumstances play a significant role. For these reasons, and because of the complications and limitations of anticoagulant therapy, antithrombotic trials have been launched with several agents which inhibit platelet function. Regarding postoperative deep vein thrombosis, neither aspirin nor dipyridamole alone appears effective, although the combination offers promise. Results with dextrans are conflicting. In recurrent idiopathic deep vein thrombosis, sulfinpyrazone may be beneficial. On the arterial side, transient cerebral ischemic attacks may be favorably affected by either aspirin or sulfinpyrazone. Prevention of thromboembolism associated with prosthetic heart valves appears possible with combination warfarin-dipyridamole therapy, and the beneficial effect of sulfinpyrazone on shortened platelet survival in this group suggests that this agent may also be effective. Sulfinpyrazone may also be beneficial in preventing thrombosis in arteriovenous canulas. The issue which has attracted the greatest attention and about which no clear answer exists at present is whether antiplatelet agents can modify the course of acute myocardial infarction. Several trials with aspirin are currently underway, and it would be premature to recommend its use in this condition until the results of these trials are available, probably in 1975.
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PMID:Platelet inhibition in the management of thrombosis. 461 23